Cadmium (Cd) is a noxious heavy metal widely dispersed in aquatic systems. Parental Cd exposure of fish species at environmental concentrations has been shown to cause deformities and stunted growth in their offspring. However, the long-term effects and the mechanisms underlying parental Cd exposure in fish species on Cd sensitivity in their offspring remain unclear. To explore the impacts of parental Cd exposures on Cd sensitivity, rare minnow (Gobiocypris rarus) larvae whose parents were exposed to Cd at 0, 5 or 10 μg/L for 28 days were established. Results showed that parental Cd exposure in rare minnow increased the Cd content of its larvae. In terms of malformation rate, mortality rate and total length at 7 days of rare minnow larvae, parental Cd exposure at 5 or 10 μg/L reduced Cd sensitivity. Further mechanistic investigation demonstrated that parental Cd exposure significantly upregulated the expression of antioxidant gene regulated by nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-кB) in rare minnow larvae. In addition, parental Cd exposure significantly elevated the level of reactive oxygen species (ROS) and malondialdehyde (MDA), but markedly decreased catalase (CAT), superoxide dismutase (SOD) and oxidized glutathione (GST) activity. The impact of parental Cd exposure to metallothionein (MT) content and the expression of MT mRNA, a detoxifying metallothionein, showed that parental Cd exposure of rare minnow induced oxidative stress in the larvae. Meanwhile, these results indicated that parental Cd exposure in rare minnow reduced the Cd sensitivity of the larvae via activating the Nrf2-mediated antioxidant system. This project helps us to further understand the toxicological mechanism of Cd in fish species and properly assess its potential ecological risk.

In recent years, zinc oxide nanoparticles (ZnO NPs) have gained attention as feed additives due to their high bioavailability. However, research on their impact on fish growth and health is limited. To investigate the influences of dietary addition of ZnO NPs on growth performance and immune function of rare minnow, rare minnows were fed diets with different ZnO NPs content. Growth analysis showed that ZnO NPs had a negative effect on the weight of rare minnow, decreasing and then increasing condition factors (CFs) and specific growth rate. Additionally, the accumulated zinc (Zn) level was significantly higher (p < 0.05), and the liver injury index was significantly higher (p < 0.05) in the dietary ZnO NPs group compared to the control group. The number of erythrocytes and leukocytes in blood samples increased and then decreased after treatment with ZnO NPs. It was further found that ZnO NPs as a dietary supplement significantly increased the Zn content and markedly repressed the expression of growth‐related genes after 60 days of accumulation in muscle tissues, and accumulation in liver tissues for 60 days significantly enhanced the expression of immune modulation–related genes expression (p < 0.05). The findings suggested that short‐term supplementation of ZnO NPs could positively affect fish growth and immune function. However, prolonged supplementation of dietary ZnO NPs resulted in reduced body weight and compromised immune function owing to the buildup of Zn in different tissues.

Zinc oxide nanoparticles (ZnO NPs) measuring 30 ± 10 nm in diameter are utilized in various applications, including batteries, plastics, ceramics, cosmetics, flame retardants, and food. However, their potential impact and risk on aquatic ecosystems remain unclear. This study examined the hepatotoxic effects of dietary ZnO NPs in rare minnow. Three hundred rare minnows were fed diets containing 0 mg/kg, 20 mg/kg and 60 mg/kg of ZnO NPs for 60 days, with hepatotoxicity assessments at 15-day intervals. The histological data showed that ZnO NPs severely damage liver tissues, causing cytoplasmic vacuolization and irregular or missing nuclei. The treatment groups showed a significant rise in the liver injury index (P < 0.05). Moreover, there was a notable increase in zinc accumulation in the ZnO NPs groups compared to the control group (P < 0.05). ZnO NPs also reduced body weight and hepato-somatic index (HSI) in rare minnows. The enzyme activity results showed elevated levels of reactive oxygen species (ROS), total cholesterol (T-CHO), triglyceride (TG), acetyl Coa carboxylase (ACC), and fatty acid synthase (FAS) in the ZnO NPs fed groups, while total antioxidant capacity (T-AOC) and malondialdehyde (MDA) decreased. Further investigation found that accumulation of ZnO NPs in the liver tissues up-regulated the levels of genes related to antioxidant (mn-sod, cat and nf-κb), pro-apoptotic (bax) and lipogenesis (gpat3, dgat1a and dgat1b), while down-regulating genes associated with lipid catabolism (cpt1 and tpi1). These findings suggest that dietary ZnO NPs cause hepatotoxicity by inducing oxidative stress through ROS, triggering apoptosis, and inhibiting lipid peroxidation. The results indicate that ZnO NPs may pose a significant threat to aquatic animals and ecosystems.

The polylactic acid (PLA), a kind of biodegradable plastic (BP), is widely used in various industries due to its environmental friendliness. Microplastics (MPs) derived from incomplete degradation of PLA presents significant ecological and health risks to aquatic organisms. However, the potential toxic mechanism of PLA MPs on intestines is still unclear. In the present study, rare minnows (Gobiocypris rarus) were exposed to 0 µg/L, 4.5 µg/L and 18 µg/L PLA MPs for 15 d. The results showed that PLA MPs exerted slight influence on intestinal growth in rare minnows, but caused intestinal damage as evidenced by intestinal villous epithelial cells eroded and necrotic, gap of edematous mucosal layer increased and fibrosis, and significantly increased inflammatory related genes expression. Moreover, the incidence and severity of intestinal damage escalated in a concentration-dependent manner, accompanied with the severe deterioration at distal intestines. Additionally, PLA MPs exposure caused intestinal mitochondrial dysfunction, as evidenced by significantly increased mitochondrial reactive oxygen species (ROS) and markedly decreased adenosine triphosphate (ATP) contents and mitochondrial respiratory enzymes activities (p < 0.05). The further studies found that PLA MPs exposure activated intestinal oxidative stress, as evidenced by significantly increased intestinal ROS and malondialdehyde (MDA), markedly decreased antioxidative stress enzyme activities and decreased antioxidative related genes expression. And then, the expression of pro-apoptotic related genes was significantly increased in PLA MPs exposure groups compared with the control levels, but decreased in the anti-apoptotic gene. Moreover, inhibited Sesn2/Nrf2 pathway may promote mitochondrial dysfunction by amplifying oxidant responses and apoptosis under PLA MPs exposure. Taken together, environmental PLA MPs aggravated intestinal damage through Sesn2/Nrf2 pathway-mediated mitochondrial dysfunction. These findings reveal a specific molecular pathway for PLA MPs to induce intestinal damage, which will contribute to assessing the ecological risks of BMPs to aquatic organisms.